RA-associated atherosclerosis: mechanisms of development and therapeutic perspectives

Abstract

According to data from large population trials and meta-analyses, mortality in rheumatoid arthritis (RA) significantly exceeds that in the general population. Cardiovascular diseases (CVD) rather widely contribute to the excess mortality in RA patients. Despite the recent emergence of a large number of innovative drugs for RA treatment, CVD mortality in this pathology persists at the level of the cardiovascular risk (CVR) typical for diabetes mellitus. With that, currently there is a clear trend among physicians for underestimating CVR in these patients. The review analyzes discovered pathogenetic mechanisms of CVR development in RA, which are represented by an integrated complex of vascular (endothelial dysfunction), cellular (T-cell dysfunction), and humoral (proinflammatory mediators, autoantibodies, complement activation) disorders. Besides, despite a large amount of disease-modifying antirheumatic drugs that can provide CVR decrease due to selective effects on separate mechanisms, the current lack of comparative trials does not allow to readily define specific drugs that are beneficial for the specific CVD decrease. Due to this, the promising trend of applied clinical medicine presumes the implementation of the interdisciplinary approach to CVR correction in RA patients, which will account not only for the treatment administered by the rheumatologist, but also the risk stratification, patient compliance, and multidisciplinary treatment efficacy control. This will allow for optimal CVD prevention in RA patients, thus significantly improving their quality of life and prognosis.